Transcription factor LSF (TFCP2) inhibits melanoma growth

Yuji Goto; Ichiro Yajima; Mayuko Kumasaka; Nobutaka Ohgami; Asami Tanaka; Toyonori Tsuzuki; Yuji Inoue; Satoshi Fukushima; Hironobu Ihn; Mikiko Kyoya; Hiroyuki Ohashi; Tamihiro Kawakami; Dorothy C. Bennett; Masashi Kato

doi:10.18632/oncotarget.6230

Transcription factor LSF (TFCP2) inhibits melanoma growth

Yuji Goto, Ichiro Yajima, Mayuko Kumasaka, Nobutaka Ohgami, Asami Tanaka, Toyonori Tsuzuki, Yuji Inoue, Satoshi Fukushima, Hironobu Ihn, Mikiko Kyoya, Hiroyuki Ohashi, Tamihiro Kawakami, Dorothy C. Bennett, Masashi Kato

Research output: Contribution to journal › Article › peer-review

24 Citations (Scopus)

Abstract

Late SV40 factor 3 (LSF), a transcription factor, contributes to human hepatocellular carcinoma (HCC). However, decreased expression level of LSF in skin melanoma compared to that in benign melanocytic tumors and nevi in mice and humans was found in this study. Anchorage-dependent and -independent growth of melanoma cells was suppressed by LSF overexpression through an increased percentage of G1 phase cells and an increased p21^CIP1 expression level in vitro and in vivo. Anchorage-dependent growth in LSF-overexpressed melanoma cells was promoted by depletion of LSF in the LSF-overexpressed cells. Integrated results of our EMSA and chromatin immunoprecipitation assays showed binding of LSF within a 150-bp upstream region of the transcription start site of p21CIP1 in melanoma cells. Taken together, our results suggest potential roles of LSF as a growth regulator through control of the transcription of p21^CIP1 in melanocytes and melanoma cells as well as a biomarker for nevus.

Original language	English
Pages (from-to)	2379-2390
Number of pages	12
Journal	Oncotarget
Volume	7
Issue number	3
DOIs	https://doi.org/10.18632/oncotarget.6230
Publication status	Published - 2016
Externally published	Yes

All Science Journal Classification (ASJC) codes

Oncology

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10.18632/oncotarget.6230

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title = "Transcription factor LSF (TFCP2) inhibits melanoma growth",

abstract = "Late SV40 factor 3 (LSF), a transcription factor, contributes to human hepatocellular carcinoma (HCC). However, decreased expression level of LSF in skin melanoma compared to that in benign melanocytic tumors and nevi in mice and humans was found in this study. Anchorage-dependent and -independent growth of melanoma cells was suppressed by LSF overexpression through an increased percentage of G1 phase cells and an increased p21CIP1 expression level in vitro and in vivo. Anchorage-dependent growth in LSF-overexpressed melanoma cells was promoted by depletion of LSF in the LSF-overexpressed cells. Integrated results of our EMSA and chromatin immunoprecipitation assays showed binding of LSF within a 150-bp upstream region of the transcription start site of p21CIP1 in melanoma cells. Taken together, our results suggest potential roles of LSF as a growth regulator through control of the transcription of p21CIP1 in melanocytes and melanoma cells as well as a biomarker for nevus.",

author = "Yuji Goto and Ichiro Yajima and Mayuko Kumasaka and Nobutaka Ohgami and Asami Tanaka and Toyonori Tsuzuki and Yuji Inoue and Satoshi Fukushima and Hironobu Ihn and Mikiko Kyoya and Hiroyuki Ohashi and Tamihiro Kawakami and Bennett, {Dorothy C.} and Masashi Kato",

year = "2016",

doi = "10.18632/oncotarget.6230",

language = "English",

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T1 - Transcription factor LSF (TFCP2) inhibits melanoma growth

AU - Goto, Yuji

AU - Yajima, Ichiro

AU - Kumasaka, Mayuko

AU - Ohgami, Nobutaka

AU - Tanaka, Asami

AU - Tsuzuki, Toyonori

AU - Inoue, Yuji

AU - Fukushima, Satoshi

AU - Ihn, Hironobu

AU - Kyoya, Mikiko

AU - Ohashi, Hiroyuki

AU - Kawakami, Tamihiro

AU - Bennett, Dorothy C.

AU - Kato, Masashi

PY - 2016

Y1 - 2016

N2 - Late SV40 factor 3 (LSF), a transcription factor, contributes to human hepatocellular carcinoma (HCC). However, decreased expression level of LSF in skin melanoma compared to that in benign melanocytic tumors and nevi in mice and humans was found in this study. Anchorage-dependent and -independent growth of melanoma cells was suppressed by LSF overexpression through an increased percentage of G1 phase cells and an increased p21CIP1 expression level in vitro and in vivo. Anchorage-dependent growth in LSF-overexpressed melanoma cells was promoted by depletion of LSF in the LSF-overexpressed cells. Integrated results of our EMSA and chromatin immunoprecipitation assays showed binding of LSF within a 150-bp upstream region of the transcription start site of p21CIP1 in melanoma cells. Taken together, our results suggest potential roles of LSF as a growth regulator through control of the transcription of p21CIP1 in melanocytes and melanoma cells as well as a biomarker for nevus.

AB - Late SV40 factor 3 (LSF), a transcription factor, contributes to human hepatocellular carcinoma (HCC). However, decreased expression level of LSF in skin melanoma compared to that in benign melanocytic tumors and nevi in mice and humans was found in this study. Anchorage-dependent and -independent growth of melanoma cells was suppressed by LSF overexpression through an increased percentage of G1 phase cells and an increased p21CIP1 expression level in vitro and in vivo. Anchorage-dependent growth in LSF-overexpressed melanoma cells was promoted by depletion of LSF in the LSF-overexpressed cells. Integrated results of our EMSA and chromatin immunoprecipitation assays showed binding of LSF within a 150-bp upstream region of the transcription start site of p21CIP1 in melanoma cells. Taken together, our results suggest potential roles of LSF as a growth regulator through control of the transcription of p21CIP1 in melanocytes and melanoma cells as well as a biomarker for nevus.

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EP - 2390

JO - Oncotarget

JF - Oncotarget

IS - 3

ER -

Transcription factor LSF (TFCP2) inhibits melanoma growth

Abstract

All Science Journal Classification (ASJC) codes

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